Biomol Ther.  2015 Mar;23(2):141-148. 10.4062/biomolther.2014.117.

Cardamonin Suppresses TGF-beta1-Induced Epithelial Mesenchymal Transition via Restoring Protein Phosphatase 2A Expression

• Kim EJ
• Kim HJ
• Park MK
• Kang GJ
• Byun HJ
• Lee H
• Lee CH

• KMID: 2380347
• DOI: http://doi.org/10.4062/biomolther.2014.117

Abstract

Epithelial mesenchymal transition (EMT) is the first step in metastasis and implicated in the phenotype of cancer stem cells. Therefore, understanding and controlling EMT, are essential to the prevention and cure of metastasis. In the present study, we examined, by Western blot, reverse transcription polymerase chain reaction (RT-PCR), and confocal microscopy, the effects of cardamonin (CDN) on transforming growth factor-beta1 (TGF-beta1)-induced EMT of A549 lung adenocarcinoma cell lines. TGF-beta1 induced expression of N-cadherin and decreased expression of E-cadherin. CDN suppressed N-cadherin expression and restored E-cadherin expression. Further, TGF-beta1 induced migration and invasion of A549 cancer cells, which was suppressed by CDN. TGF-beta1 induced c-Jun N-terminal kinase (JNK) activation during EMT, but CDN blocked it. Protein serine/threonine phosphatase 2A (PP2A) expression in A549 cancer cells was reduced by TGF-beta1 but CDN restored it. The overall data suggested that CDN suppresses TGF-beta1-induced EMT via PP2A restoration, making it a potential new drug candidate that controls metastasis.

Keyword

Cardamonin; Epithelial mesenchymal transition; TGF-beta1; JNK; PP2A; A549

MeSH Terms

Adenocarcinoma
Blotting, Western
Cadherins
Cell Line
Epithelial-Mesenchymal Transition*
JNK Mitogen-Activated Protein Kinases
Lung
Microscopy, Confocal
Neoplasm Metastasis
Neoplastic Stem Cells
Phenotype
Polymerase Chain Reaction
Protein Phosphatase 2*
Reverse Transcription
Transforming Growth Factor beta1
Cadherins
JNK Mitogen-Activated Protein Kinases
Protein Phosphatase 2
Transforming Growth Factor beta1